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TITLE: Spasmodic Dysphonia: Evaluation and Management
SOURCE: Grand Rounds Presentation, UTMB, Dept. of Otolaryngology
DATE: March 10, 2009
SENIOR MEDICAL STUDENT: Olvia Revelo
FACULTY ADVISOR: Michael Underbrink, MD
SERIES EDITOR: Francis B. Quinn, Jr., MD, FACS
ARCHIVIST: Melinda S. Quinn, MSICS
"This material was prepared by resident physicians in partial fulfillment of educational requirements established for
the Postgraduate Training Program of the UTMB Department of Otolaryngology/Head and Neck Surgery and was
not intended for clinical use in its present form. It was prepared for the purpose of stimulating group discussion in a
conference setting. No warranties, either express or implied, are made with respect to its accuracy, completeness,
or timeliness. The material does not necessarily reflect the current or past opinions of members of the UTMB faculty
and should not be used for purposes of diagnosis or treatment without consulting appropriate literature sources
and informed professional opinion."
INTRODUCTION
Spasmodic dysphonia (SD) is a focal, adult-onset dystonia of the intrinsic laryngeal
muscles. It is characterized by intermittent phonatory breaks during speech occurring secondary
to laryngeal muscle spasms. Patients with SD typically manifest their symptoms when
attempting voluntary speech. Individuals may be asymptomatic at rest or during reflexive
phonation such as coughing, crying, laughing, and yawning. Symptoms may fluctuate during
singing or whispering. Although the cause of SD is still unknown, it seems to be associated with
certain triggers, illnesses, and environmental factors. Spasmodic dysphonia has been associated
with other focal dystonias such as blepharospasm, torticollis, and Writer’s Cramp. Neurological
disorders such as Parkinson’s and amyotrophic lateral sclerosis have also been associated with
SD. Finally, environmental factors such as certain infections, trauma, stress or even medications
have been suspected to trigger SD.
Spasmodic dysphonia affects approximately 1:10,000 Americans with a peak age of
onset between 35-45 years of age. It has a greater tendency to affect females, with the female to
male ratio ranging from 3:1 up to 8:1. A positive family history exists in approximately 12
percent of affected population.
There are two main types of SD, adductor spasmodic dysphonia (ADSD) and abductor
spasmodic dysphonia (ABSD). In some rare instances both types of symptoms are present in
which case it is said to be mixed. Some authors believe both types are present in all patients with
symptoms depending on the predominance of either the adductor or abductor type.
There are nine cartilages that make up the larynx: thyroid, cricoid, epiglottic, and paired
arytenoids, corniculate and cuneiform. The thyroid cartilage is composed of two lamina that
come together on the anterior side of the cartilage to form the laryngeal prominence. The
posterior edge of each lamina articulates with the cricoid cartilage inferiorly at the cricothyroid
joint. Movement of the cartilage at this joint produces a change in tension at the vocal folds,
which in turn produces variation in pitch of the voice. The longer the vocal fold, the higher the
pitch (effect of length is offset by increase in tension). The entire superior edge of the thyroid
cartilage is attached to the hyoid bone by the hyothyroid membrane. Another important landmark
is a small prominence on the internal surface of the thyroid cartilage midline which is the
attachment point for the anterior commissure of the vocal folds.
The cricoid cartilage is the only complete ring of cartilage around the trachea. It
attaches superiorly to the thyroid cartilage and inferiorly to the trachea. The function of the
cricoid is to provide attachments for the various muscles, cartilages, and ligaments involved in
opening and closing the airway and in speech production.
The pair of arytenoid cartilages rest upon and articulate at the base with the superior
edge of the cricoid cartilage. They consist of two processes: the vocal process to which the vocal
ligament attaches to, and the muscular process which serves as an insertion point for several
laryngeal muscles.
The laryngeal muscles can be classified into two types: intrinsic and extrinsic.
Intrinsic muscles act directly upon the arytenoids except for the cricothyroid muscle that acts
indirectly, and the extrinsic or accessory muscles which are involved in the elevation and
depression of the larynx. The posterior cricoarytenoid muscles which attach inferiorly with the
posterior surface of the cricoid cartilage and superiorly to the muscular process of the arytenoid
cartilage are the only abductors of the vocal cords. The lateral cricoarytenoid and transverse
arytenoid muscles are both involved in adducting the vocal folds. The thyroarytenoid muscle
shortens the vocal cords and consequently changes the frequency of vocal fold vibration. The
cricothyroid muscle controls vocal fold lengthening and pitch.
There are two different neurologic pathways involved in voice production one being
voluntary and the other involuntary. Corticobulbar fibers from the cerebral cortex descend
through the internal capsule and synapse on the motor neurons in the nucleus ambiguus. The
nucleus ambiguus is the area within the brainstem (medulla) from which arise the fibers that will
contribute to the vagus nerve. Lower motor neurons leave the nucleus ambiguus and travel
laterally, exiting the medulla between the olive and the pyramid as a series of eight to ten
rootlets. These rootlets coalesce into the vagus nerve, which then exits the skull base via the
jugular foramen. The vagus nerve descends in the carotid sheath, giving off three major
branches: the pharyngeal branch, the superior laryngeal nerve (SLN), and the recurrent laryngeal
nerve (RLN). The SLN supplies sensation to the glottic and supraglottic larynx, as well as motor
input to the cricothyroid muscle. The RLN arises from the vagus nerve in the upper chest and
loops under the aortic arch on the left and subclavian artery on the right and ascends back into
the neck traveling in the tracheoesophageal groove. The nerve enters the larynx posteriorly,
adjacent to the cricothyroid joint. The RLN supplies all of the intrinsic laryngeal muscles with
the exception of the cricothyroid muscle. This pathway summarizes the voluntary pathway for
voice production.
Etiology of SD remains unknown. Historically this disorder has been considered
psychogenic in nature but current theory involves a neurologic cause. Evidence supporting this
theory include knowledge of basal ganglia involvement in other focal dystonias and the
development of SD after head trauma.
Diagnosis is based on history and careful examination of the glottis across a variety of
laryngeal tasks. Spasmodic dysphonia must be distinguished from other functional voice
disorders such as voice tremor. An underlying neurologic disease must also be ruled out
especially Wilson’s, Huntington’s and Parkinson’s disease which may cause secondary SD.
Typical features on history include deterioration of voice quality under stress or on
telephone, and improvement with sedatives such as alcohol and benzodiazepines. Singing or
laughing will sometimes result in greater fluency, probably due to the task-specific nature of
dystonia.
One author defined “idiopathic spastic dysphonia” by the following criteria: 1. patient
must exhibit the voice signs of SD, 2. there must be an absence of vocal cord lesions or paralysis,
3. patient must exhibit normal remaining peripheral speech mechanisms, and 4. resistance of
symptoms to voice therapy and psychotherapy.
Clinical features can help distinguish between the different types of SD. Adductor type
SD (ADSD) is found in about 85 percent of diagnosed cases in the United States. The most
common symptom associated with adductor type SD is a choked, strained-strangled voice with
abrupt breaks in phonation in the middle of vowels. Breaks are due to hyper adduction of the
vocal folds resulting in a quick glottic closure interrupting airflow through the glottis and
interrupting phonation. Patients may experience difficulties with continually voiced sentences
particularly when glottal stops mark word boundaries like “we_eat,” or when two voiced sounds
occur in sequence within the word such as “ye_ar” or “d_og”. Examples of sentences patients
may have a difficulty with include “We eat eels every day”, “We mow our lawn all year” and “A
dog dug a new bone”.
Abductor type SD (ABSD) is less common, found in approximately 15 percent of
patients with SD. Patients usually exhibit a breathy, effortful voice with abrupt breaks resulting
in whispered elements of their speech characterized by excessive and prolonged abduction
during voiceless consonants (/h/,/s/,/f/,/p/,/t/,/k/). Vocal fold abduction interferes with closure of
the vowel sound that follows. To examine for symptoms of abductor SD the patient’s speech
should be compared during voiced sentences such as “We mow our lawn all year,” which should
contain few abnormalities, with sentences containing a high proportion of voiceless consonants
such as “The puppy bit the tape” and “When he comes home we’ll feed him”. If severe enough,
the patient may display complete aphonia.
Mixed type SD is extremely rare. Patients display symptoms of both adductor and
abductor type SD. Diagnosis of a mixed disorder is important for predicting response to
treatment. Diagnosis is similar to the diagnosis of either type of SD, with patients having
difficulties with both types of tasks. Mixed patients are difficult to treat as Botulinum toxin can
produce unwanted side effects with no benefit. Thyroarytenoid injection produces breathiness
that exacerbates the disorder, while injection to the posterior cricoarytenoid muscle may provide
little benefit.
Diagnosis:
Diagnosis can be verified using electromyography, fiber optic laryngoscopy,
videostroboscopy, aerodynamic testing, and vocal spectrographic analysis. Examination during
connected speech is most likely to reveal the involuntary laryngeal motion that causes symptoms.
That is why the larynx is best examined with a flexible nasopharyngoscope. Insertion of
laryngeal mirror or rigid endoscope combined with the necessary traction of the tongue may
mask the features. Diagnosis is based on speech symptoms and must be distinguished from
functional voice disorder, and an underlying neurologic disease must be ruled out.
Treatment:
Botox:
There is no known cure for SD. Different types of therapy have been used to battle this
debilitating condition including pharmacotherapy, voice therapy, and even surgery. The gold
standard treatment for SD is Botulinum toxin (BTX). This toxin prevents presynaptic release of
acetylcholine (ACH) at the neuromuscular junction. It is important to note that different
serotypes of botulinum toxin exhibit specific proteolysis of proteins involved in transport and
binding of Ach vesicles to presynaptic membranes. This reaction results in a temporary paralysis
of the muscle involved. Historically, BTX injections have been used to successfully treat other
focal dystonias including blepharospasms and torticollis. This led researchers to develop
protocols for the treatment of SD, and in 1984 Blitzer et al applied it to SD. It is currently the
gold standard treatment due to its mild side effects, easier technique, and cheap cost compared to
the rest of the treatment modalities. Surgical interventions are typically reserved for patients who
do not respond to Botox treatment or develop resistance to it. There are 8 distinct subtypes of
Botulinum toxin that exist (A, B,C1, C2, D, E, F, G). Types A and B are the only subtypes
manufactured for clinical use: type A Botox (Dysport), and type B Myobloc (Neurobloc).
Paralysis from botulinum toxin can be overcome in 2 ways: production of accessory axonal
terminals, or by production of new proteins by the cell.
In more detail, botulinum toxin binds to the neuronal cell membrane at the nerve
terminus and enters the neuron by endocytosis. The light chain of botulinum toxin cleaves
specific sites on the SNARE proteins, preventing complete assembly of the synaptic fusion
complex and thereby blocking acetylcholine release. Botulinum toxins types B, D, F, and G
cleave synaptobrevin; types A, C, and E cleave SNAP-25; and type C cleaves syntaxin. Without
acetylcholine release, the muscle is unable to contract.
Treatment with BTX results in the reduction in voice breaks usually by 48 hours post
treatment. Treatment lasts an average of 3-4 months before recurrence of symptoms. The most
common side effect is breathiness. Other side effects include: dysphagia, prolonged voice loss,
aspiration, hoarseness, pain at injection site and stridor (with PCA injection). Usually no overt
changes are noted for the first 48 to 72 hrs. The effects of toxin can continue to increase up to
seven days after injection, probably because of diffusion of toxin through the muscle. This may
be why some patients with ADSD report that their voice is best three days after an injection in
the thyroarytenoid muscle, followed by the onset of breathiness and other side effects by day
five. Breathiness can last 1-2 weeks and may be more pronounced following bilateral injection.
Dysphagia for liquids may occur, with symptoms usually dissipating within 3-5 days. During the
affected time period, patients should be advised to sip through a straw and to avoid attempting to
swallow liquids quickly. Side effects can often be minimized with lower dosing, but may be a
trade off as the duration of effects may also be shortened. Dosage-side effect profile is very
individual among patients. There are no absolute contraindications for the use of BTX injections
and they may be used safely in children. Since unknown potential for teratogenicity on neonates
and infants, use in pregnant or lactating women is not advised. Aminoglycosides may potentiate
effects of the toxin.
Patients with known reflux should be treated with anti-reflux medications because,
theoretically, the slowed vocal fold closure after injection may predispose them to aspiration.
Unfortunately, 3 – 5% of patients undergoing BTX injection have developed resistance to the
toxin. This is believed to occur by development of antibodies. Risk factors for developing
immunogenicity include use of higher doses, shorter intervals between injections (<3 months),
booster doses, and young age. There is no assay to test for presence of antibodies. Some centers
confirm resistance by injecting 15 U of BTX into one side of the frontalis muscle with retained
symmetry indicating resistance. Resistant patients can sometimes be treated with other toxin
serotypes. BTX is supplied in crystallized powder form which should be diluted in preservative
free saline before use.
There are several techniques used to inject BTX into the vocal cord muscles for
treatment of ADSD. In one method, a percutaneous injection is guided by EMG signals obtained
through use of a teflon-coated hollow needle. The needle is inserted through the thyrocricoid
membrane (located through palpation) and directed upward toward the contralateral
thyroarytenoid muscle (TA). By having the patient phonate and observing and hearing the
resultant EMG interference pattern when the needle comes in contact with the desired muscle,
we can ensure correct positioning. During the procedure the patient is asked not to cough or
swallow to prevent movement of the needle once in the TA.
Alternate injection techniques for ADSD include the transoral laryngoscopic approach,
transnasal laryngoscopic approach, and transcartilaginous “point touch” injection technique.
Techniques which allow for other means of locating the injection site were developed in an effort
to increase the accuracy with which toxin could be administered while eliminating the need for
EMG monitoring for injection. The transoral approach involved indirect visualization of the
vocal folds via standard laryngoscopic procedure. The vocal folds are anesthetized through the
application of a topical cocaine solution. BTX is then injected along the superior margin of the
vocal folds.
The transnasal technique uses a flexible nasolaryngoscope with a working channel that
is equipped with a flexible catheter needle. Topical phenylephrine and lidocaine are sprayed
transnasally, then the scope is introduced. Once in place, lidocaine solution drip is applied to the
surface of the vocal folds via the working channel while the patient phonates to prevent airway
penetration or aspiration. The needle is inserted through the surface of the thyroid cartilage
halfway between the thyroid notch and inferior edge. Following insertion the needle is passed
through the cartilage and into TA muscle where BTX is injected. All methods yield comparable
results. Technique chosen is very patient and physician dependent.
The injection technique for abductor type SD requires access to the posterior
cricoarytenoid muscles. In this approach, the larynx is rotated manually away from the injection
site. The needle is passed posterior to the posterior edge of the thyroid and then advanced
toward the posterior plate of the cricoid cartilage and positioned in the PCA under EMG
guidance. The patient is asked to sniff to contract the posterior cricoarytenoid muscles and verify
correct position. There is usually sufficient response by weakening just one posterior
cricoarytenoid muscle.
Blitzer et al. (1999) reported their 12 year experience with BTX with more than 900
patients with SD. Ninety percent of patients with ADSD and 66.7% with ABSD achieved a
normal voice after injection. Injection after nerve section failure showed up to 81%
improvement. However these patients never did as well as those who have never undergone
surgery and their perception of improvement was lower on average. Patients with combined
abnormalities only had 30% improvement.
Advantages of using BTX include: a less invasive procedure than surgery, no
permanent damage to nerve or laryngeal structures, temporary nature allows for dosage
adjustments, and wide availability. Some disadvantages of BTX are the need for repeated
injections, the unpredictable relationship between dosage and response, risk for resistance to
treatment, and the adverse side effects associated with treatment.
Pharmacological Treatment:
No controlled studies have demonstrated effective symptom control using
neuropharmacology. Examples of agents used include beta blockers such as propranolol, the
anticholinergic trihexyphenidylHCl (Artane), and benzodiazepines like diazepam and
alprazolam. The role of this pharmacology has been to provide relief without any demonstrable
symptom reduction. However, clinicians often have individual patients who have reported
significant symptom relief. At present the role of these medications in the management of SD is
only as an adjunct to other approaches.
Voice Therapy
Voice therapy is another approach to treatment which has unfortunately not had any
demonstrated effectiveness in treating SD. It may help rule out a psychogenic disorder and may
be used to provide support for those who do not benefit from Botox (mild symptoms). Some
patients use it in adjunct to Botox to prolong symptom free periods. Traditional voice therapy
approaches for ADSD employ techniques for avoiding overpressure. Breathy voice onsets,
reduced speech force, using a head focus, and laryngeal manipulation are all techniques aimed at
reducing laryngeal tension. Therapy can also use relaxation and respiration training to help gain
insight and control of laryngeal tension during speech.
Surgical Treatment:
The first surgical technique used to try and correct SD was recurrent laryngeal nerve
section described by Dedo in 1976. His first publication was a case series in which he described
the outcomes of 34 patients who underwent RLN section. They observed that RLN paralysis
retracts the involved vocal cord from midline (in the paramedian position) so the normal fold
fails to reach as firmly as usual, causing a breathy but often phonatory soft voice. Dedo first tried
lidocaine injections on one of his patients who was relieved of the spasms and agreed to undergo
RLN section for a more permanent relief. He then sectioned the RLN in 34 patients after
temporary paralysis with Xylocaine showed significant improvement in vocal quality. They
treated patients with unilateral RLN section thinking that the creation of unilateral vocal cord
paralysis could prevent hyper adduction and loss of speech fluency at the cost of the dysphonia
associated with paralysis.
In his 1991 publication, a retrospective review of pre and post operative recordings of
300 patients who underwent RLN section. Patients answered questionnaires regarding voice
production and voice recordings were analyzed by perceptual voice evaluation and acoustic
analysis of voice spectra. Fifteen percent of the patients were reported to have developed
recurrence of mild to moderate spasticity 6 to 24 months after RLN section. Eighty-two percent
had little or no voice spasticity 5 to 14 years after RLN section. Since then, this approach has
been abandoned by most laryngologists in favor of the reliability of BTX injections.
Aronson and DeSanto (1983) followed 33 patients for 3 years post RLN section.
Thirty-six percent of patients maintained improved voices on follow up. Of the 64% failed
voices, 48% were worse than before surgery. They concluded that the effectiveness of unilateral
RLN section for severe ADSD decreases with time and results in voice failure in a sizeable
percentage of patients. They postulated that return of symptoms was not due to reactivation of
the vocal cords, but rather hyper adduction of the normal vocal folds alone or along with other
muscles of the supraglottis and extrinsic musculature. Since this study RLN section was widely
abandoned for the simpler BTX injection method for temporary relief of SD symptoms.
In 1991 Netterville et al reported on a modification of the RLN surgery after a patient
who developed recurring adductor spasm 1 year after section was reexplored with identification
of neural regrowth into the distal segment of the RLN. In this modification the RLN was
followed distally toward the intrinsic laryngeal muscles and then avulsed. They theorized that
with this technique, neural re-growth would be diminished and recurrence of SD symptoms
would be reduced. He published a retrospective review of 12 patients with no recurrence at 1.5
years after surgery. A follow up report in 1996 of 18 patients followed for 3-7 years post RLN
avulsion showed 16 of 18 patients were without spasm. The most common side effect reported
was breathy voice. The remaining patients had minimal spasm and six underwent medialization
laryngoplasty to improve voicing. The RLN avulsion procedure hold promise in management of
SD patients not responsive or tolerant to BTS injections, but still at the cost of the breathy
dysphonia associated with unilateral vocal cord paralysis. Further research still needs to take
place before recommending this on a regular basis.
Currently there are several surgical techniques being explored for the treatment of SD
but are still considered experimental. These procedures include recurrent laryngeal nerve
denervation and reinnervation , type II thyroplasty , and posterior cricoarytenoid myoplasty with
medialization thyroplasty.
In 1999 Berke was the first to describe a technique for selective bilateral RLN
denervation followed by reinnervation with the ansa cervicalis. The procedure specifically
denervates the laryngeal adductors and spares the abductors. This allows treatment of both sides
of the larynx without compromising the patient’s airway function. In this procedure, a modified
thyroplasty type window is created bilaterally. This window is situated more posteriorly and
inferiorly than for a thyroplasty. The intrinsic RLN is visualized as it courses toward its
terminus in the TA muscle. Verification of the anatomy is made by intraoperative evoked EMG
performed with nerve stimulation and custom made endotracheal tube that places surface
electrodes on the vocal cord mucosa. The PCA branch is protected behind a strut of the inferior
cornu of the thyroid cartilage. This branch is not disturbed. The nerve is then dissected under
magnification, and branches to the TA and LCA are isolated. The TA and LCA branches are
lysed, and then using microneurosurgical technique, the sternohyoid branch of the ansa cervicalis
is sutured to the distal TA branch of the RLN. In this fashion reinnervation of the TA can occur
with a nerve that is uninvolved by SD. This reinnervation preserves the tone of the TA muscle
and gives the patient improved voicing when the muscle reinnervates. This controlled
reinnervation prevents aberrant reinnervation by the severed RLN stump, an unwanted result
observed in the original Dedo treated patients. The proximal RLN stump is sutured outside the
thyroid cartilage and the cartilage window is closed to prevent aberrant reinnervation. In his
initial report in 1999 Berke presented preliminary results of 21 patients who had been followed
up a median of 36 months. At that time 19 of 21 patients had absent to mild dysphonia, and only
1 underwent post operative BTX treatment.
In his 2006 paper, Berke gives long term follow up results for the procedure. The
study is a retrospective analysis of surgical outcome with average follow up interval of 49
months. Surgical outcome was evaluated using patient surveys and perceptual voice analysis.
Out of 136 patients, 83 returned surveys with 91% satisfied with fluency of voice. Forty-six
patients provided voice recordings for perceptual evaluation, results showed 26% had voice
breaks, and 30% breathiness. Limitations for the study include a high dropout rate (61%), small
sample size, and lack of long term prospective studies. Attributable advantages of the procedure
include the permanence of treatment effect and less breathiness due to maintenance of vocal fold
tone from ansa cervicalis innervation. Disadvantages to consider are the technical difficulty of
the surgery, recurrence of symptoms, and lack of reproducibility. A prospective study is
underway.
Midline lateralization thyroplasty, otherwise known as thyroplasty type II, was proposed
by Isshiki et al for treatment of SD. In their 2001 retrospective review of 6 SD patients, 5 out of
6 patients obtained near normal voices. The concept is to decrease adductory forces by changing
the anatomy of the larynx. Since there is an excess glottal closure during spasms leading to
dysphonia the procedure makes an effort to control the degree of glottal closure to obtain a
predictable voice result. Isshiki performs a midline incision in the thyroid cartilage dividing the
thyroid ala. Each ala is then lateralized and this position is maintained by either a silicone shim
placed over a muscle spacer, or they have recently created a titanium bridge. To achieve
additional vocal cord lateralization, the anterior commissure is divided with a needle to create a
tiny defect and a composite cartilage graft is placed to prevent granuloma formation.
A big advantage of the procedure is that it does not deprive the patient of nerve or
muscle function. Failures were attributed to difficulty in lateralization and concurrent focal neck
dystonia. Limitations include small sample size, no current long term prospective studies, and
no objective measurements were described.
Midline lateralization thyroplasty was proposed by Chan in 2004. He published a
prospective case series with 13 subjects. He used the same method described by Isshiki, but his
results showed that 9 of 13 patients failed and 2 had their surgery reversed. Reasons for failure
were unclear, especially when they had good early results after surgery. They presume that with
time vocal fold hyper adduction is able to overcome the initial lateralization created by the shims
because the underlying neuropathology has not been resolved. Limitations of the study include
the small study sample, the use of self-rating assessments and no objective measures.
Advantages of this type of surgery are that an optimal glottal closure can be adjusted and
readjusted, there is no damage of physiologic function, and it is reversible. Some disadvantages
described include the technical difficulty of the surgery and shim displacement, the fact that it
does not relieve the cause of SD, and lack of reproducibility.
Posterior cricoarytenoid myoplasty with medialization thyroplasty was proposed by
Shaw in his 2003 case report of 3 patients with ABSD. Three patients refractory to BTX were
treated with the surgery one unilaterally, and the other two bilaterally. The patient’s voices were
analyzed both with subjective surveys and perceptual voice analyzed in different intervals up to a
year. Their voices were recorded and a blinded speech pathologist listened for prolonged
voiceless consonants. These patients were treated with surgery and followed up to a year post
surgery. The procedure consists of approaching the PCA insertion in the muscular process of the
arytenoid through a window in the posterior part of the thyroid ala. Then disinsertion of the
muscle is done and a plastic sheet is placed and secured between the elevated muscle and
arytenoid cartilage to prevent reinsertion. Once the sheet is adequately positioned and secured, a
medialization thyroplasty is performed. All patients reported improved subjective symptoms and
showed objective reduction in phonatory breaks. The unilaterally treated patient had to undergo
the procedure on the opposite sides due to recurrence of symptoms after 6 months. There was no
airway compromise or other post operative complications. Obviously larger sample and follow
up needed. Medialization thyroplasties have been tried in the past to treat ABSD with only short
lived improvement. As stated earlier, there is less success with BTX treatment for patients with
ABSD. This procedure is proposed for these refractory patients.
Summary
Spasmodic dysphonia is an idiopathic disorder of the larynx. The mainstay of treatment
continues to be BTX injections into the laryngeal muscles. BTX treatment is not perfect; there is
an onset time characterized by a breathy voice and dysphagia and an offset time characterized by
recurrence of symptoms. Occasionally patients can develop antibodies and resistance. Some
patients do not like to receive multiple injections a year. Because of these shortcomings,
alternative, more permanent treatments have been sought. Surgery for ASDS was initially
developed in the 1970s but has been abandoned because of poor long term results. A RLN
denervation and reinnervation and laryngoplastic techniques may hold promise for long term
treatment. All current therapies for SD are directed toward the symptoms of the disorder. There
is still work toward understanding the underlying cause so we can then possibly develop a cure
for the disease.
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